Medfools Bacteriology a la chart for the USMLE I

Adapted from notes from UCLA., with additional corny mnemonics

Staphylococcus aureus

(virulent)

(nonmotile, nonsporeforming, facultative anaerobe)

Gm+ cocci

Diseases

Characteristics

Habitat/Transmission

Pathogenesis

Diagnosis

Treatment

Prevention

*Skin infections:
impetigo, cellulitis,
erysipelas, abcess,
furuncle, carbuncle
*Bacteremia/sepsis:
hematogenous spread
*Acute endocarditis:
DESTRUCTIVE (compare
to S.viridans and
S.faecalis)
*Pneumonia damaging
process, cavitations,
empyema, effusions
*Osteomyelitis/septic
arthritis- hematogenous
and traumatic spread
*Food poisoning 1-8 hr
onset, vomiting, preformed
toxin
*Tox shock syndromefever, vomiting, diarrhea,
diffuse erythematous rash

Gm + cocci in
grapes/clusters

Ubiquitous in
environment; normal
flora of skin/nose

Enterotoxin- vomiting,
diarrhea, heat resistant,
(actually released in gut)
TSST-1 tampon use,
wounds, superantigen
Exfoliatin- scalded skin

Gm + cocci in grapes,
Catalase differentiates
from Strep.

Beta lactamase
production is
common! Use
methicillin,
nafcillin,
dicloxacillin

none

Catalase +
coagulase +

Spread through lesions,

fomites

TISSUE SPREAD:
Alpha toxin(lechthinase)skin necrosis;hemolysis
Hyaluronidase- degrades
proteoglycans
Fibrinolysin- lysis fibrin
clots
IMMUNE EVASION:
Protein A- binds IgG-Fc,
blocks opsonization and
complement fixation
Coagulase- activates
prothrombin
Hemolysin- destroys
RBCs, PMNs, M0s,
platelets
Leukocidin- destroys
WBCs

S.aureus: Beta
hemolysis, coagulase,
Yellow (Au) pigment
(coagulase causes
coagulation!)

MRSAvancomycin

Coagulase neg:
S. epidermidis:
novobiocin sensitive
sensitive skin
S. saprophyticus:
Novobiocin resistant

S. epidermitis: associated w/ IV catheters, damaged/prosthetic heart valves: INSIDIOUS onset, Nosocomial, LESS virulent.
Blood culture Contaminant
S. saprophyticus: Community acquired UTI in young women

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Streptococcus viridans (GABHS) (nonmotile, nonsporeforming)

Gm+ cocci

Diseases

Characteristics

Habitat/Transmission

Pathogenesis

Diagnosis

Treatment

*Pharyngitis- strep throat,

erythema, tonsillar exudate, fever
*Skin/soft tissue infectionsimpetigo, cellulitis, necrotizing
fascitis
*Scarlet fever- centrifugal, red
rash, erythrogenic toxin, slap cheek,
strawberry tongue
*Tox shock syndrome- clinically
like Staph TSS
*Rheumatic fcver- fever,
myocarditis, polyarthritis, chorea,
subcutaneous nodules, erythema
marginatum rash. Mitral valve
disease follows pharyngitis, NOT
skin infections. Abs vs. bacteria
cross react w/ joint and heart
antigens
*Acute GN- hypertension,
hematuria, edema of face/ankles.
Follows both pharyngitis AND skin
infections. Cross reactive antigens
deposited in GBM.

Gm + cocci in
chains or pairs

Human throat/skin,
Transmission by
respiratory droplets

Hyaluronidase- degrades
proteoglycans
(TISSUE SPREAD)
Erythrogenic toxinscarlet fever, lysogenized
S.pyogenes
Streptolysin 0- results in
beta hemolysis, target of
ASO antibodies

All Strep are

Catalase

Penicillin to
prevent
rheumatic
fever.

Beta-hemolytic are
classified by
Lancefield groups
(A,B,D) according
to Ccarbohydrates

Beta hemolysis
and Bacitracin
sensitivity point to
GABHS, esp with
inc. ASO titer.

Prevention

Penicillin
DOES NOT
treat post strep
disease or
enterococcus.

M protein- antibody
target, but inhibits
complement/phagocytosis
Streptokinase- converts
plasminogen to plasmin,
dissolves fibrin clots
IgA protease
HES an MSI

S. agalactiae (Group B strep)

Neonatal menigitis, sepsis
pneumonia

Beta-hemolytic

Female urinary tract

S. faecalis (enterococcus)
Subacute endocarditis, UTI
Oh crap! Ive got Heart
problems!

Not hemolytic

GI tract

Grows in 6.5% NaCl

Not hemolytic

GI tract

Hydrolyze esculin in presence of

bile. NOT grow in 6.5% bile

S. bovis (group D)
UTI

S. pneumoniae

(pneumococcus)

Lobar pneumonia, ADULT

meningitis, URI (kids)

Alpha-hemolytic

Nasopharynx

85 different capsular
polysaccarides

Quellung rxn

23 valent vaccine, for

AIDS, elderly, asplenics

S. Mutans , mitis (Viridans group)

Subacute endocarditis, caries

Alpha-hemolytic

Oropharynx

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Neisseria

(Chocolate agar, Oxidase +, kedney bean shape)

Gm- cocci

N. meningitidis (meningococcus)
Diseases

Characteristics

Habitat/Transmission

Pathogenesis

Diagnosis

Treatment

Prevention

*Meningococcemia- fever,
arthralgias, myalgias,
petechial rash, inc. in
people w/ complement
deficiencies
*meningitis- fever,
headache, stiff neck,
photophobia, inc.PMNs in
CSF
* WaterhouseFriedrichsen- fever,
purpura, DIC, adrenal
insufficiency due to
bilateral adrenal
hemorrhage, shock, death
(like a bad
meningococcemia)

Gm cocci kidney
beans.

Airborne droplets,
colonized nasopharynx,
establishes carrier states
in some

Polysaccharide capsule,
endotoxin (LPS),
IgA protease

Ferments maltose

Penicillin or
Ceftriaxone
(G3)

Chemoprophylaxis
with Rifampin
(excreted into
saliva)

Thayer-Martin,
chocolate agar

Capsular polysaccharides
are antigenic serve as
markers for classification.

N. gonnorhoeae (gonnococcus)
Males- symptomatic
dysuria, penile discharge
b/c of urethritis. Leads to
epididymitis, prostatitis,
urethral strictures
Female- asymptomatic,
vaginal discharge,
dyspareunia, due to
cervicitis, Infertility, PID,
ectopic, tubo-ovarian
abcess, perihepatitis (FitzHugh-Curtis syndrome),
opthalmia neonatorum

Polysaccharide
vaccine in military
recruits.

LATEX agglutination
test b/c capsular
polysaccharides

(most common notifiable disease in US)

NO CAPSULE

Sexual transmission

Gm cocci kidney
beans.

OFTEN coexistent WITH

Chlamydia AND
Syphilllis (tx w/
tetracycline or
chloramphenacol)

Thayer-Martin,
chocolate agar

Presumptive diagnosis
by Gm stain of
petechiae or CSF

Pili/fimbriae
(ANTIGENIC variation)

Men: Gm diplococci
in PMNs

LPS
OMPs
IgA protease

Does NOT ferment

maltose

NO CAPSULE!

No serologic testing, no
capsule!

Ceftriaxone
(G3) b/c
penicillinase
producing
N.gonnorhoeae
PPNG common

Erythromycin
eye drops in
newborns (also
protects vs.
Chlamydia)
No Vaccine.

Both: Septic arthritis

NOTE: bacterial meningitis: 0-6 months (Group B Strep, E.coli, Listeria); 6 months 3 years (H.influenzae B),
3-15 years (N. meningitidis), >15 years (S. pneumoniae)

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Clostridium

Gm+ Rods

(Anaerobic, spore-forming, with Exotoxin)

C. tetani
Diseases

Characteristics

Tetanus tetany, risus

sardonicus joker smile,
exaggerated reflexes,
respiratory failure

Habitat/Transmission

Pathogenesis

Spores, ubiquitous in
soil, enter wounds and
germinate in anaerobic
environment of necrotic
tissue

Tetanus toxin travels

intra axonally to CNS,
blocks release of
inhibitory glycine
neurotransmitter

Diagnosis

Treatment

Prevention

Penicillin,
ventilatory
support, muscle
relaxants

Tetanus
toxoid
(formaldehyde
treated tox)

Tetanus immune
globulin,
preformed Ig

C. botulinum
Botulism flaccid paralysis,
descending weakness, diplopia,
flaccid paralysis, resp failure.
Wound botulism- spores to
wounds, germinate, release toxin
Infant botulism- ingestion of
spores in honey- floppy baby

Spores, in soil,
inadequate sterilization
of canned foods.
Alkaline veggies,
smoked fish.

Botulinum toxin ingested

preformed. Tox spreads
in blood, to nerves blocks
Ach RELEASE

Antitoxin,
ventilatory support

Watch swollen
cans!

NO
PENICILLIN!!
Will burst cells
and release toxin

Toxin can be used to Tx

torticollis, blepharospasm

C. perfingens
Gas gangrene (myonecrosis):
war wounds, septic abortions
Food poisoning- ingestion of
cooking resistant spores in
foods. Watery diarrhea,
cramps, little vomiting

Results in
crepitus- gas
production and
Hemolysis

Normal flora of colon

and vagina

Alpha tox- lecithinase

degrades cell membraneshemolytic

Morphology,
exudate smears,
culture, sugar
fermentation,
organic acid
production

Debridement, O2
gas, Penicillin

Normal flora in 3% of
people

Suppression of normal
flora allows overgrowth,
usually by clindamycin,
ampicillin,
cephalosporins
Exotox A (severe
diarrhea
Exotox B (damage to
colonic mucosa)

ID C-diff tox in
stool

Metronidazolepoorly absorbed
orally, inc. colonic
dose

C. difficile
Antibiotic associated
pseudomembranous colitis- esp
in hospitalized pts.

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Vancomycin

Bacillus

Gm+ Rods

(Aerobic, spore-forming, with Exotoxin)

B. anthracis
Diseases

Characteristics

Habitat/Transmission

Pathogenesis

Diagnosis

Treatment

Prevention

Woolsorters diseasepulmonary anthrax, pneumonia

Large w/ square
ends, nonmotile

Common in animals.
Humans infected by
spores on animal
products (skins/hides)

Antiphagocytic capsule
made of d-glutamate
[only one w/ Amino
acids!] (not a
polysaccharide)

Morphology and
blood agar growth.

Penicillin

Sterilization of
animal
products, and
vaccination of
animals.

Transmission through
skin, GI tract, respiratory
tract

Vaccine
(protective
antigen) for
humans at risk

Tripartite anthrax
toxin: protective
antigen, lethal factor,
edema factor. Protective
factor inhibits
phagocytosis.

B. cereus
Vomiting with 4 hr incubation
period (like S.aureus)- heat
stable toxin--

Distinguished
from B. anthracis
by motility and
lack of capsule.

Corynebacterium diptheriae

Spores on grains survive

cooking and germinate
when food is warmed.

Treat symptoms

Preformed heat-labile
enterotoxin (like E.coli,
Cholera tox) - diarrhea

Avoid
reheated rice

Gm+ Rods

(nonmotile, nonsporeforming, Chinese)

Diseases

Characteristics

Habitat/Transmission

Pathogenesis

Diagnosis

Treatment

Prevention

Diptheria throat
inflammation, gray
fibrinous exudate
(pseudomembrane), airway
obstruction, myocarditis,
recurrent laryngeal nerve
palsy

Club shaped, in
palisades, Chinese
characters

Airborne droplets,
colonization of throat and
production of Diptheria
tox.

Diptheria tox: inhibits

protein syn by ADP
ribosylation of
eukaryotic ef-2. Toxin
produced by lysogenized
bacteria (like erythrogenic
toxin of GABHS)

Tellurite plate,
Loefllers

Antitoxin,
Penicillin to
reduce
transmission

Diptheria toxoid
vaccine. (disease in
US is iatrogenic
due to innoculation
by inadequately
killed toxin.

Polyphosphate
granules stain
metachromatically

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Toxin assessed by
animal inoculation or
gel diffusion precipitin
test.

Listeria monocytogenes

Gm+ Rods

(Facultative intracelluar anerobes, Non-sporeforming, tumbling motility)

Diseases

Characteristics

Habitat/Transmission

Pathogenesis

Diagnosis

Treatment

Prevention

Neonatal meningitis and

sepsis, abortion, premature
delivery

Gm + rods, in
clumps, Chinese
characters, NONsporeforming,
Tumbling
distinguishes it
from
corynebacterium

Newborns,
immunocompromised are
high risk groups.

Only Gm+ with LPS

Infects monocytes and
induces granulomas.
Listeriolysin O punches
holes in cells

Gm+ rods, beta

hemolysis, motility

Ampicillin

No vaccine

Transmitted to humans
from animal feces,
veggies, unpasteurized
milk/cheese.

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ENTERIC GRAM NEGATIVE RODS

Note: Not all gram negative enterics belong to Enterobacteriaciae family: 1) colonic location 2) facultative anaerobes 3)ferment
glucose, 4)oxidase negative, and 5)reduce nitrates to nitrites. ALL are members here EXCEPT: Vibrio, Campylobacter,
Helicobacter, Pseudomonas, Bacteriodes. (Vile People Cant Be Happy) As a group, Enterobacteriaciae are often normal flora.
Pathogenisis is by endotoxin/LPS, exotoxins. O (Outer polysaccharides), H (flagHella), K (Kapsular polysaccharides) are important
antigens. Inoculation on MacConkeys or Eosin-Methylene Blue (EMB) agar differentiates family members by lactose fermenting
ability. Fermenters are pink-purple, non-fermenters are colorless. Also keep an eye on motility.

ENTERIC
E. coli

Gm- Rods

(Intestinal AND non-Intestinal disease)

(Enterobacteriaciae)

Diseases

Character

Hab/Trans

Pathogenesis

Diagnosis

Treatment

Prevent

Most common UTI, Gm- sepsis, travellers

diarrhea. 2nd most common cause of
Neonatal meningitis.
Enterotoxigenic strains: Do NOT invade!
heat labile enterotox binds GM1 ganglioside
receptor, activates adenylate cyclase via
ADPribosylation of G protein. (like Cholera
tox) Watery diarrhea.
Enterohemorragic: verotoxin inhibits 60s
ribosome (like Shigella) Bloody diarrhea.
0157:H7 type causes hemolytic-uremic
syndrome (anemia, thrombocytopenia, renal
failure) associated w/ fast food outbreaks
Enteroinvasive: factor mediated invasion of
epithelial cells, sepsis. Bloody diarrhea with
WBCs.

As other

Normal flora,
but need
virulence
factors to cause
disease.

Pathogenisis by pilus
and enterotox,
capsule, and
endotoxin.

Ferments lactose, unlike

Salmonella, Shigella

G3 Cephalosporin

No vaccine

Does NOT ferment

lactose. Production of
H2S gas distinguish from
Shigella.

S. typhi- by Cipro
or ceftriaxone

Hand
washing,
cooking,
water
chlorination

Salmonella

enterobacteria
ciae family

Serotype ID by O,H,K
antigens

(Enerobacteriaciae)

S. enteritidis causes gasteroenteritis via

Cholera like tox. Large inoculum needed.
(Peptic acid kills) Tx symptoms.
S.typhi Typhoid fever, init by asymptomatic
infection of gut phagocytes and dissemination
to liver, Gall bladder (carrier state), Fever,
RLQ abdominal pain, rose spots. Tx Cipro or
ceftriaxone.
S. cholerae-suis- Gm- sepsis. Esp patients
with Sickle cell (risk for osteomyelitis b/c
func. Asplenia)

As other
enterobacteria
ciae family

Normal flora of
animals.
Contamination
food, poultry /
eggs

K anitgen/Vi antigen
Flagella antigenic
variation

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ENTERIC
Shigella

Gm- Rods

(INTESTIAL disease)

(Enterobacteriaciae)

Diseases

Characteristics

Habitat/Transmission

Pathogenesis

Diagnosis

Treatment

Enterocolitis (dysentary) by
S.dysentariae, S.sonnei, S.
flexneri, S. boydii

Nonmotile

Not normal flora. Humans

only host. 4Fs: fingers
flied food feces (fecaloral)

Distal ileal and colonic

mucosal invasion and
cell death. Does NOT
enter bloodstream
(unlike Salmonella)

NO H2S gas,
nonmotile. Non
lactose fermenting
on EMB,
MacConkeys agar

Fluid replacement,
avoid
antiperistaltic
drugs which
prolong excretion
of organism.

Small innoculum
<100 bugs

Prevention

PMNs in smear w/
fever suggest
invasive bug.

Vibrio

(Not Enterobacteriaciae)

Cholera - Massive watery

diarrhea (Rice water stool) like
enterotoxic E.coli

Comma shaped,
single flagella.
Large innoculum
needed.

Infects humans only,

transmission by fecaloral.

V.parahemolyticus is a marine
bug in contaminated raw
seafood. Japan

Campylobacter

Gastritis, peptic ulcer, risk

factor Gastric carcinoma

Diagnosis clinically
in endemic areas:
Asia, Africa, Latin
America.

Oral rehydration

No effective
vaccine.

Antibiotics

No Vaccine

Bismuth sulfate,
tetracycline,
metronidazole

No vaccine.

(Not Enterobacteriaciae)

More frequently causes

enterocolitis than Salmonella
or Shigella. Can cause bloody
diarrhea

Helicobacter pylori

Mucinase aided
colonization of small
intestine, bipartite
enterotox: binds GM1
gangliosides on
enterocyte, ADPribosylation of G
protein. (like ETEC)

Comma or Sshaped,
Microaerophilic,
urease negative

Domestic animals via

fecal oral, unpasteurized
milk

Probably
enterotoxin

Blood agar w/antibiotics,

C.jejuni grows at 42C,
produces oxidase,
nalidixix acid sensitive
C.intestinalis grows at
25C, oxidase neg,
resistant to nalidixic acid

(Not Enterobacteriaciae)
Urease + (protects
from stomach
acid)

Fecal-oral.

Attaches to gastric
mucosa, mediated by
NH3 production, host
inflammatory response

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ENTERIC

Gm- Rods

(EXTRAINTESTIAL disease)

Klebsiella-Enterobacter-Serratia

(Enterobacteriaciae)

Diseases

Characteristics

Habitat/Transmission

Opportunistic pathogens cause UTI,

pneumonia, usually nosocomial
Klebsiella is nonmotile, with
capsule, mucoid colony appearance.
Klebsiella pneumo renowned for
severity, bloody currant jelly
sputum, lung cavitations.
Serratia- bright red pigment.
Nosocomial- Ab resistant

All ferment
Lactose

Large intestine, soil water

Pathogenesis

Diagnosis

Treatment

Prevention

Ferment lactose on
EMB, MacConkeys
agar

No vaccine

Swarming appearance
on blood agar. Use
antigens from
Rickettsiae cross react
with Proteus.

No vaccine

K.pneumoniae,
E.cloacae,
S.marcescens
difficult to
distinguish
clinically

Proteus-Providencia-Morganella (Enterobacteriaciae)
Community and nosocomial UTI,
b/c high motility
(important species:
Proteus mirabilis, Proteus vularis
Providencia rettgretii
M. morganii )

Pseudomonas

Non lactose
fermenting,
urease +
(alkalinizes urine)

Large intestine, soil water

Only enterobac
that makes
phenylalanine
deaminase

P.mirabilis is indole
neg unlike others of
this group.

(Not Enterobacteriaciae)

P aeruginosa: opportunistic,
nosocomial: Pneumonia,
osteomyelitis, burn infections,
sepsis, UTI, endocarditis, malignant
otitis externa, corneal infections.
P. cepacia colonizes CF patients

Bacteroides fragilis
Peritoneal abscesses. Growth
favored by growth w/ facultative
anaerobes to exhause local oxygen

Strict aerobe,
Not glucose
fermenting, Not
reduce nitrates,
oxidase +

Normal flora of colon.

Exotox like
C.diptheriae
(ADPreibosylation)

Produces pyocyanin,
pyoverdin

Highly resistant.
Combo pipercillin,
ticarcillin and
aminoglycoside.
Ceftazidime

(Not Enterobacteriaciae)
Anaerobic, non
sporeforming,
non LPS,
polysaccharide
capsule. No
exotox, No LPS

Predominant flora of
colon. NOT communicable.
Exits colon via break in
mucosa (Chronic disease,
PID, trauma)

Polysaccharide
capsule
provides
virulence factor

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Treat as mixed
infection.
Clindamycin, or
metronidazole

No Vaccine

RESPIRATORY
H. Influenzae
Diseases

Gm- Rods

(chocolate agar w/ heme and NAD)

Characteristics Habitat/Transmission

Leading cause of meningitis in

kids. Peak at 6m to 1 yr. (decline
in maternal IgG, inability of
infants to mount attack vs.
polysaccharide capsule)

Coccobacillus w/
polysaccharide
Capsule

Upper respiratory tract,

respiratory droplets

Fatal epiglottitis by type B

influenzae.

Pathogenesis

Diagnosis

Treatment

Prevention

ONLY encapsulated
forms like type B cause
invasive disease.
Nonencapsulated cause
URI, pneumonia in pts
with preexisting lung
disease (COPD).
IgA protease,

Chocolate agar,
w/ heme and
NAD.

Rifampin
prevents
meningitis and
transmission
from close
contacts b/c
secreted into
saliva better than
Ampicillin

HIB vaccine of
capsular
polysaccharide
conjugated to
carrier protein.

Erythromycin
(also good for
Mycoplasma)

Disinfect water
sources

Erythromycin
reduces
complications,
doesnt change
clinical course.
Resp tract
already
damaged.

Killed B.pertussis
vaccine 2,4,6
months, Boosters
at age 1, school.
Acellular vax for
booster only.

Quellung rxn

Hmmmm
Chocolaaate!

H.Simpson

Legionella pneumophilia
Atypical pneumonia with high
fever, nonproductive cough(
differentiate from Mycoplasma,
influenza, psittacosis, Q fever)

Bordetella pertussis
Whooping cough- acute
tracheobronchitis with URI
symptoms, paroxysmal
hacking cough 1-4 wks,
copious mucus

(Cysteine and Iron agar)

Poor gm stain

Airborne from water

sources. Smoking EtOH,
Immunosuppressed are
at risk.

High concentration
Error! No table of
figures entries
found.of cysteine
and iron. Urine
antigen test.
Suspect when inc.
PMNs with no
organisms!

(Bordet-genou agar)
Small gm- rods

Airborn droplets (highly

contagious)

Polysaccharide capsule
and pili are essential for
virulence. Does NOT
invade. Pertussis tox
(ADP-ribosylation), and
tracheal cytotoxin.

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Culture on Bordetgenou agar. Ab

agglutination, stain

10

ZOONTIC

Gm- Rods

Brucella (virulent, facultative intracellular, tx: aminoglycoside)

Diseases

Characteristics

Habitat/Transmission

Pathogenesis

Diagnosis

Treatment

Prevention

Brucellosis- influenza like

syndrome w/ undulating
fever(higher during day, lower
at night). Lymphadenopathy,
H/Smegaly, no boboes/ulcers.

Small gm- rods

Animal reserviors:
B melitensisi (goats/sheep)
B. abortus (cattle)
B. suis (pigs)
Non pasteurized milk
products(travelers),
through skin (meat
packers, vets, farmers)

Organisms localize in
RES. Persist in
macrophages, induce
granulomas

Serology,
biochemistry

Antibiotics

Animal
vaccination,
pasteurization.

Francisella tularensis
Tularemia- influenza like
syndrome w/ ulceroglandular
lesions (hole in skin, black base,
swollen LN, draining pus)

Yersinia pestis

No Human
vaccine.

(virulent, facultative intracellular, tx: aminoglycoside)

Small gm- rods

Ubiquitous in US in wide
variety of animals.
Tick/mite vectors.
Humans as accidental dead
end hosts by bites or
animal skin handling.

Enters through skin,

localizes in RES.
Persist in macrophages,
induce granulomas

Serology

Streptomycin

Live
attenuated
vaccine (like
BCG)

Immunoflorescence

Antibiotics

Quarantine.

(virulent, facultative intracellular, tx: aminoglycoside)

Plague- Hematogenous spread

results in fever myalgias,
hemorrhage. Also septic shock,
pneumonia.

Small gm- rods

with bipolar stain

Endemic in prairie dogs in

US, 99% cases in SE Asia.
Rats/flease in urban
centers. Also woundperson respiratory
droplets.

Bacteria spread to
regional LN, enlarged
tender buboes.

No Vaccine.

Pasteurella multocida
Cellulitis rapid onset at bite
site. Osteomyelitis as
complication. Sutures
predispose to infection

Small gm- rods

Normal flora of dogs and

cats. Transmitted to
humans by animal bite.

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Presumptive Dx by
rapid onset cellulitis
at animal bite.

Penicillin

Ampicillin
prophylax.

11

MYCOBACTERIA

(Obligate aerobe, facultative intracellular organisms)

Acid Fast Rods

M. tuberculosis
Diseases

Character

Habitat/Transmission

Pathogenesis

Diagnosis

Treatment

Tuberculosis: chronic low

grade fever, night sweats,
productive cough, hemoptysis,
weight loss. Elderly,
immunocomp, malnourished at
risk.

Obligate
aerobe,
intracellular,
infect M0,
persist for
years.
Mycolic
acid walls

Only infects humans. Respiratory

aerosol. Infects M0s in mid/lower
lobes, init granuloma formation,
widely disseminate the infection. T
cells help M0 kill some intracellular
mycobacteria at expense of
bystander cell damage. Result:
necrotic host cells, viable
mycobacteria. Walled off w/ giant
cells, fibroblasts, collagen,
calcification to form granuloma or
tubercle. This 1 infection = Ghon
focus on CXR (when including Ca
tubercles in perihilar lymph nodes =
Ghon complex.) Reactivation
prefers upper lobe (obligate
aerobe) of lung. Reactivation can
infect any organ. Cervical LN
(scrofula),spine (Potts disease.)

Mycolic acids confer

acid fastness. WaxD is
active ingredient in
Freunds adjuvant.
Cord factor is
virulence factor
(mycoside= 2 mycolic
acids + disaccharide)

PPD tests for prior

exposure or to BCG
vax. Positive test if
both redness,
induration 48-72
hr after injection
(DTH rxn.)

Prolonged,
multiple Tx.
(INH, rifampin,
pyrazinamide,
ehtambutol)

Note: candida and

mumps as controls
in immunocomp.
Acid fast stain.
NaOH concentrate
on LowensteinJensen medium.
Slow culture, 6-8
wks. Niacin
production

Protracted tx
b/c: intracellular
life cycle,
granuloma
blocks
penetration of
drug,
metabolically
inactive
mycobac persist
in lesion

Prevention
Chemoproph
ylax w/ INH
(watch
hepatotox in
people >35
y.o.)
Live
attenuated
M.bovis
(BCG)
induces some
protective
immunity.

M. avium- intracellulare
Clincal TB indistinguishable
from M tuberculosis in AIDS.

Atypical
mycobacterium

Found in water, soil, not

pathogenic in guinea pigs
(infects birds)

Azithromycin
Clarithromycin

Macrolide
prophylax
when CD4
count < 50

Rifampin
Dapsone
Up to 2 years!

Prophylax
exposed
persons with
Dapsone.

M. leprae
Leprosy- preferential growth in < 37C,
skin, superficial nerves.
Tuberculoid- good cellular immune
response, few AFB, granulomas,
positive lepromin skin test. Anethetized
skin lesions and thickened superficial
nerves.
Lepromatous- poor cellular immune
response, lots of organisms, foamy
histiocytes, negative lepromin skin test
(poor response.) Skin lesions, lion
facies. Skin anesthesia, bone resorption,
skin thickening, disfiguring.

Never has
been
grown in
lab.

Brazil, India, Sudan

Humans only natural hosts.
Mouse footpad and
armadillo growth only.
Transmission by nasal
secretions, skin lesions to
persons with prolonged
contact w/pts.

Intracellular replication
(skin histiocytes,
endothelial cells,
Schwann cells)

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12

ACTINOMYCETES

Gm- Branching Rods

A. israelii
Diseases

Characteristics

Habitat/Transmission

Pathogenesis

Diagnosis

Treatment

Prevention

Actinomycosis- hard nontender swelling, drains pus

through sinus. (abscess that
spreads to neck, chest,
abdomen.)

Aanerobic Gmbranching rods

Normal anaerobic flora

oral cavity/GI tract. Not
communicable.

Invasion after local

trauma (risk factor for
anaerobic growth)

Anaerobic Gmbranching rods,

sulfur granules in pus

Penicillin

No vaccine

Acid fast branching,

NO sulfur, aerobic

Bactrim
(trimethorprim +
sulfamethoxazole)

No vaccine

Nocardia asteroides
Nocardiosis- pneumonia
that progresses to abscess
formation, sinus tract
drainage, dissemination to
brain/kidney
(immunosuppressed)

(Acid Fast Branching)

Aerobic Gmbranching rods.

Mycoplasma pneumoniae

Soil, NOT normal flora

Small free living organism

(No cell wall, poor gm stain)

Diseases

Characteristics

Habitat/Transmission

Pathogenesis

Diagnosis

Treatment

Prevention

Walking pneumonia
(dry nonproductive cough,
horrible CST, generally
feel well) Most common
pneumonia in young
adults (college students).

Smallest free living

organism, no cell
wall so poor gm
stain, resists
penicillins,
cephalosporins.
Cell membrane has
chol which are not
in other bacteria.
Fried egg
colonies on Eatons
agar. (Eat Fried
Eggs w/ chol)

Respiratory droplets.
Attaches but does NOT
invade respiratory
epithelium, like
B.pertussis.

Pathogenic only for

humans.

Elevated titer of cold

agglutinins or specific
anitbodies

Erythromycin
Tetracycline

No vaccine

Arrests cilliary motion,

induces epithelial cell
necrosis. Cross reactive
antigens induce anti RBC
autoantibodies (cold
agglutinins.)

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13